Cardiometabolic multimorbidity has become an increasingly urgent global public health concern. Patients rarely develop these disorders in isolation; hypertension begets atherosclerosis, diabetes accelerates vascular injury, and stroke and ischemic heart disease frequently follow. What ties this cluster together, the review emphasizes, is endothelial dysfunction, a failure of the single-cell layer that lines every blood vessel in the body. The endothelium is far more than a passive barrier. It regulates vascular tone through nitric oxide signaling, controls inflammatory adhesion of immune cells, maintains the integrity of barriers such as the blood-brain barrier, and orchestrates tissue repair. When it falters, the consequences ripple across the entire cardiovascular and metabolic system, which is why endothelial dysfunction serves both as an early warning marker and as a central driver of disease progression.

The review’s central proposition is that endothelial cells communicate their state of health, or distress, to distant tissues through extracellular vesicles, particularly exosomes. These nanoscale membrane-bound particles, typically ranging from roughly 30 to 150 nanometers in diameter, are released when multivesicular bodies within the cell fuse with the plasma membrane. Far from being cellular debris, exosomes are carefully sorted packages carrying a molecular cargo that mirrors and modulates the physiology of the parent cell. Endothelial-derived exosomes, abbreviated ECs-exo in the review, transport microRNAs, long non-coding RNAs, circular RNAs, proteins, and lipids to recipient cells, where these molecules can reprogram gene expression, alter signaling pathways, and shift cellular behavior.

The mechanistic detail assembled by the Chongqing team is considerable. Dysregulated exosomal cargos, the authors report, propagate vascular inflammation, insulin resistance, and fibrotic remodeling across cardiometabolic disease. Inflammatory cascades involving Toll-like receptor 4 signaling, adhesion molecules such as ICAM-1 and VCAM-1, and mediators like high mobility group box 3 protein and oxidized low-density lipoprotein are amplified or dampened by the exosomal payload. Signaling hubs including the MAPK and ERK pathways, protein kinase C-alpha, phosphatase and tensin homologue, forkhead box protein O1, and hypoxia-inducible factor-1alpha appear repeatedly in the regulatory networks the review describes. Hypoxia-inducible factor-1alpha in particular links oxygen deprivation, a hallmark of ischemic heart disease and stroke, to exosomal reprogramming that can either aggravate injury or, under the right conditions, promote adaptation and repair.

Not all endothelial exosomes are harbingers of disease. The review highlights a protective side of the axis: exosomal microRNAs released by healthy endothelium support vascular repair and suppress pathological inflammation. Endothelial progenitor cells, which participate in vessel regeneration, release vesicles enriched with pro-angiogenic and anti-inflammatory microRNAs that can enhance nitric oxide production, reduce endothelin-1-driven vasoconstriction, and stabilize vulnerable plaques. Molecules such as heme oxygenase-1, Krüppel-like factor 2, and vascular endothelial growth factor feature in these restorative programs, while chemokine receptor type 4 helps guide reparative vesicles to sites of injury. In models of cerebral ischemia such as middle cerebral artery occlusion, endothelial and progenitor-derived vesicles have been shown to protect the blood-brain barrier, in part by preserving tight junction proteins like zona occludens 1 and modulating von Willebrand factor release and angiopoietin-2 signaling.

This dual nature, pathological messenger and therapeutic agent, is precisely what makes the exosomes-X axis clinically attractive. On the diagnostic front, the review catalogs circulating endothelial exosome signatures with potential utility for early detection, prognosis, and disease stratification. Because exosomes in the blood carry molecular fingerprints of their cells of origin, profiling their microRNA, protein, and lipid content offers a non-invasive window into vascular health. A blood test that reads the endothelial exosome cargo could, in principle, identify patients at risk of developing multimorbidity long before symptoms appear, distinguish between inflammatory and metabolic disease subtypes, and track response to therapy over time. The authors argue that such signatures hold genuine promise as biomarkers, though they note that standardization of isolation and analytical methods remains an obstacle to clinical deployment.

On the therapeutic side, the review evaluates an emerging strategy: engineering endothelial exosomes to deliver therapeutic cargos and thereby restore vascular homeostasis. Exosomes offer several advantages over synthetic drug carriers. They are naturally biocompatible, cross biological barriers including the blood-brain barrier, can be surface-functionalized with targeting ligands, and can be loaded with RNA therapeutics, anti-inflammatory proteins, or small molecules. The authors describe multimodal formulations and advanced bioengineering platforms designed to tune vesicle tropism, cargo loading efficiency, and release kinetics. Engineered vesicles derived from healthy endothelium or endothelial progenitor cells could, for example, deliver anti-inflammatory microRNAs to atherosclerotic plaques or insulin-sensitizing cargos to metabolically active tissues, addressing several facets of multimorbidity with a single platform.

The concept of theragnostics, the fusion of therapy and diagnostics in one system, runs throughout the review. Because the same exosomal signatures that signal disease can be engineered into delivery vehicles that report on their biodistribution, ECs-exo could enable truly individualized treatment: profile the patient’s vesicle cargo, identify the dominant pathological pathway, select or engineer a matching therapeutic vesicle, and monitor the molecular response in circulation. The authors position this integrated approach as a way to improve diagnosis, prognosis, and personalized management of cardiometabolic multimorbidity, a condition whose complexity has largely defeated single-target drugs.

The review is candid about the challenges that stand between laboratory promise and bedside impact. Isolation and characterization protocols vary widely across studies, cargo sorting mechanisms are not yet fully mapped, dose standardization for vesicle therapeutics is unresolved, and large-scale manufacturing under good manufacturing practice conditions remains a formidable engineering problem. Distinguishing protective from pathological vesicle populations within a heterogeneous circulating pool is another unsolved puzzle. Nevertheless, the convergence of mechanistic insight, biomarker discovery, and bioengineering capability documented in the review suggests that the field is approaching an inflection point.

Funded by the National Natural Science Foundation of China, the Natural Science Foundation of Chongqing, and a Chongqing medical scientific research joint project, the work reflects a broader international push to understand extracellular vesicles as the body’s intercellular internet. If the exosomes-X axis framework proves correct, the endothelium’s nanoscale messengers may soon serve simultaneously as the earliest alarm for cardiometabolic disease, the yardstick of its progression, and the vehicle that reverses it. For the millions of people living with overlapping cardiovascular and metabolic disorders, that would represent a fundamental shift from managing separate diseases to treating the vascular system as the integrated whole it truly is.

Subject of Research: Endothelial cell-derived exosomes as diagnostic biomarkers and engineered therapeutics for cardiometabolic multimorbidity

Article Title: Exosomes-X axis: endothelial-derived extracellular vesicles for precision diagnosis and therapy in cardiometabolic multimorbidity

Article References: Tang, F., Zhu, S.-C., Zhou, H.-M., Liu, M., Yuan, W.-X., & Qiu, X.-W. (2026). Exosomes-X axis: endothelial-derived extracellular vesicles for precision diagnosis and therapy in cardiometabolic multimorbidity. Journal of Translational Medicine. https://doi.org/10.1186/s12967-026-08946-w

Image Credits: AI Generated

DOI: 10.1186/s12967-026-08946-w

Keywords: exosomes, endothelial cells, extracellular vesicles, cardiometabolic multimorbidity, type 2 diabetes, hypertension, atherosclerosis, stroke, microRNAs, endothelial dysfunction, targeted therapy, theragnostics

The investigative focus centered on the effects of amentoflavone on human umbilical vein endothelial cells (HUVECs) exposed to tumor necrosis factor-alpha (TNF-α), a potent pro-inflammatory cytokine notorious for triggering endothelial activation and promoting atherogenesis. TNF-α’s role in elevating the expression of adhesion molecules, enhancing oxidative stress, and disrupting endothelial barrier function marks it as a key driver in vascular pathology. The researchers embarked on an in-depth examination of whether amentoflavone could counteract these deleterious changes induced by TNF-α, thereby preserving endothelial integrity.

At the molecular level, TNF-α initiates a cascade of events leading to the upregulation of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin, which facilitate the adhesion and transmigration of leukocytes into the vascular intima. This leukocyte infiltration fuels inflammation and accelerates plaque formation. The novel aspect of this study lies in its assessment of amentoflavone’s ability to suppress these adhesion molecules in HUVECs, potentially interrupting the pro-inflammatory dialogue that sustains endothelial dysfunction.

Utilizing advanced cellular assays, the team observed that amentoflavone significantly attenuated TNF-α-induced expression of adhesion molecules in a dose-dependent manner. This finding not only highlights amentoflavone’s anti-inflammatory capacity but also suggests a direct interaction with the signaling pathways that govern endothelial activation. Intriguingly, the compound’s modulatory effects extended beyond mere surface molecule expression, implicating deeper influences on intracellular signaling networks associated with inflammation.

Central to the inflammatory response in endothelial cells is the nuclear factor-kappa B (NF-κB) pathway, a transcription factor that regulates the expression of numerous pro-inflammatory genes. Activation of NF-κB by TNF-α results in a sustained inflammatory milieu conducive to vascular injury. The study revealed that amentoflavone impaired the translocation of NF-κB to the nucleus, thus inhibiting its ability to activate target genes responsible for sustaining endothelial activation. This mechanistic insight underscores the therapeutic potential of amentoflavone as a modulatory agent at the genetic regulatory level.

Beyond NF-κB inhibition, amentoflavone’s antioxidant properties contributed significantly to its protective effects on endothelial cells. Oxidative stress, characterized by excessive reactive oxygen species (ROS), is a principal exacerbator of endothelial damage and a promoter of inflammatory signaling. The researchers demonstrated that amentoflavone reduced intracellular ROS accumulation induced by TNF-α, thereby alleviating oxidative burden and preventing the downstream consequences of redox imbalance in endothelial cells.

This dual anti-inflammatory and antioxidant profile of amentoflavone portends considerable benefits for the vascular system, especially under conditions that predispose individuals to atherosclerosis and thrombosis. The findings presented in this preliminary investigation pave the way for further exploration into flavonoid-based therapies as adjuncts or alternatives to current pharmacological interventions targeting endothelial dysfunction.

Complex interplay between cytokine signaling and endothelial phenotype changes is further influenced by kinases such as mitogen-activated protein kinases (MAPKs), which regulate cellular responses to stress stimuli. The study’s data suggest that amentoflavone modulates the activation of specific MAPKs, thereby tuning the endothelial cell’s response to inflammatory triggers. This layer of regulation adds a compelling dimension to the understanding of how natural compounds can precisely recalibrate pathological signaling cascades.

Corroborating the cellular findings, gene expression analyses conducted in the study provided robust evidence that amentoflavone downregulated key pro-inflammatory genes while upregulating cytoprotective ones. This genomic shift could represent a fundamental reprogramming of endothelial cells towards a more quiescent and resilient state, countering the deleterious effects usually instigated by TNF-α.

The implications of these findings reach far into the realm of cardiovascular therapeutics, positioning amentoflavone as a candidate for novel drug development that harnesses natural product pharmacology. Given the global burden of cardiovascular diseases, innovations that offer safer, efficacious options for managing endothelial health represent a critical unmet need in medicine.

Nevertheless, the authors emphasize the preliminary nature of the study and advocate for in vivo validation and clinical translation to ascertain dosage, bioavailability, and long-term safety profiles of amentoflavone. Moreover, the complexity of the vascular environment in humans, replete with myriad cell types and systemic influences, necessitates comprehensive studies beyond the simplified in vitro model of HUVECs.

In summary, this meticulous exploration into the effects of amentoflavone on TNF-α-induced endothelial activation delineates a promising natural intervention with wide-reaching implications for vascular disease prevention and treatment. By elucidating molecular targets and signaling pathways modulated by amentoflavone, the research provides a compelling narrative that aligns with the growing interest in flavonoids as modulators of inflammatory and oxidative stress mechanisms in human health.

Future research directions will undoubtedly focus on characterizing the pharmacodynamics and pharmacokinetics of amentoflavone, as well as its potential synergistic effects with existing cardiovascular drugs. Additionally, investigations into its efficacy across other types of endothelial cells and in models of chronic vascular inflammation will bolster the understanding and therapeutic applicability of this biflavonoid.

The revelation of amentoflavone’s multifaceted protective role holds promise not just for cardiovascular medicine but also for broader inflammatory disorders where endothelial activation serves as a pathological cornerstone. As the scientific community continues to unravel the complexities of endothelial biology, natural compounds such as amentoflavone stand at the frontier of innovative, integrative therapeutic strategies that combine efficacy with minimal side effects.

Overall, this study embodies a significant leap in vascular biology research, spotlighting amentoflavone as a potent, naturally derived agent capable of counteracting endothelial dysfunction by targeting the nexus of inflammatory and oxidative pathways. With cardiovascular disease remaining the leading cause of mortality worldwide, such findings ignite hope for new avenues in disease modulation and underscore the untapped potential residing within nature’s pharmacopoeia.

Subject of Research: Effects of the natural biflavonoid amentoflavone on TNF-α-induced endothelial activation in human umbilical vein endothelial cells (HUVECs).

Article Title: A preliminary investigation of the effects of amentoflavone on TNF-α-induced endothelial activation in HUVECs.

Article References:
Turk, F.C., Onal, B., Celik, Z. et al. A preliminary investigation of the effects of amentoflavone on TNF-α-induced endothelial activation in HUVECs. BMC Pharmacol Toxicol (2026). https://doi.org/10.1186/s40360-026-01143-x

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Extensive studies have delineated the molecular and cellular architecture underpinning inflammation’s role in atherosclerosis, heart failure, and other cardiovascular pathologies. The statement underscores that systemic inflammation acts as a catalyst for endothelial dysfunction, plaque instability, and myocardial remodeling. Crucially, it identifies the high-sensitivity C-reactive protein (hsCRP) assay as a widely accessible, cost-effective biomarker that quantifies systemic inflammation levels with remarkable precision. Despite ongoing debates about its clinical utility, this document distinguishes hsCRP as a valuable prognostic indicator across the spectrum of primary and secondary preventive cardiovascular care.

In comparative prognostic analyses among patients with established cardiovascular conditions, hsCRP demonstrated predictive power for future adverse cardiac events equivalent to, if not surpassing, low-density lipoprotein (LDL) cholesterol levels. This finding persists even among cohorts undergoing optimized statin therapy, which conventionally aims to reduce LDL cholesterol but does not uniformly mitigate inflammatory activity. Consequently, hsCRP assessment opens avenues for refined risk stratification and personalized therapeutic interventions targeting inflammatory pathways alongside lipid modulation strategies.

Beyond biochemical diagnostics, the Scientific Statement rigorously evaluates lifestyle factors influencing systemic inflammation. Evidence-based recommendations emphasize habitual physical activity, with a minimum threshold of 150 minutes per week of moderate-intensity exercise, as a potent anti-inflammatory modality. Furthermore, dietary regimens such as the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets are lauded for their anti-inflammatory nutrient profiles, rich in antioxidants, fiber, and unsaturated fats.

Complementing these recommendations is a spotlight on omega-3 fatty acids, specifically eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), predominantly derived from fatty fish consumption. Regular intake—up to two to three servings weekly—is stressed as a critical mediator in attenuating chronic low-grade inflammation and enhancing cardiovascular resilience. These nutritional strategies harmonize with lifestyle management protocols delineated in the 2025 ACC/AHA High Blood Pressure Guideline, reinforcing an integrative approach to vascular health.

At the cellular level, the inflammatory cascade involves complex interactions among immune cells, cytokines, and vascular endothelial cells, culminating in chronic vascular injury and pathological remodeling. The paper delves into mechanisms whereby inflammatory mediators such as interleukin-6, tumor necrosis factor-alpha, and various adhesion molecules orchestrate endothelial activation, promoting leukocyte recruitment and foam cell formation within arterial walls—hallmarks of atherogenesis.

In heart failure paradigms, inflammation interplays with neurohormonal dysregulation, precipitating maladaptive myocardial fibrosis and contractile dysfunction. The statement synthesizes emerging evidence that targeting inflammatory signaling pathways could augment conventional pharmacotherapies, potentially transforming therapeutic landscapes in heart failure management.

The scientific consensus articulated in this statement advocates for hsCRP measurement as an adjunctive tool that supplements lipid profiles, enabling clinicians to tailor interventions that encompass both lipid lowering and anti-inflammatory strategies. Ultimately, integrating inflammatory biomarkers into cardiovascular risk algorithms promises to refine prognostication and optimize patient outcomes.

The document also critically examines pharmacologic agents with anti-inflammatory properties, including novel biologics and repurposed drugs, assessing their efficacy and safety profiles in cardiovascular populations. It opens the discourse for future randomized clinical trials to elucidate the optimal integration of these agents within standard-of-care frameworks.

Notably, the ACC’s comprehensive approach in this Scientific Statement reflects a paradigm shift, championing inflammation as a modifiable cardiovascular risk factor. The synergistic incorporation of biomarkers, lifestyle modifications, and targeted therapeutics embodies a precision medicine ethos aimed at curtailing the global burden of cardiovascular disease.

Published in the Journal of the American College of Cardiology (JACC), this statement is poised to influence clinical guidelines, research trajectories, and patient care paradigms worldwide. It calls for sustained interdisciplinary collaboration between clinicians, researchers, and public health stakeholders to translate these insights into actionable strategies that alleviate cardiovascular inflammation and its sequelae.

In conclusion, the American College of Cardiology’s 2025 Scientific Statement on “Inflammation and Cardiovascular Disease” crystallizes the intricate nexus between inflammatory biology and cardiovascular pathology. As the medical community pivots towards a more nuanced understanding and management of inflammation, this landmark document equips healthcare professionals with the knowledge to harness diagnostic and therapeutic innovations that promise to revolutionize cardiovascular care.

Subject of Research: Inflammation as a pathophysiological contributor to cardiovascular diseases, including coronary artery disease and heart failure

Article Title: Inflammation and Cardiovascular Disease: 2025 ACC Scientific Statement

News Publication Date: September 29, 2025

Web References:

• Journal of the American College of Cardiology (JACC): https://www.jacc.org/doi/10.1016/j.jacc.2025.08.047
• American College of Cardiology: http://www.ACC.org

References: DOI: 10.1016/j.jacc.2025.08.047

Keywords: Cardiovascular disease, Heart disease, Heart failure, Coronary artery disease, Preventive medicine, Cholesterol, Inflammation

Heart failure with preserved ejection fraction is a distinct form of heart failure characterized by impaired relaxation of the myocardium and compromised filling of the left ventricle, despite a normal ejection fraction. Unlike heart failure with reduced ejection fraction (HFrEF), which has several evidence-backed therapies, HFpEF has baffled clinicians and researchers alike. The pathophysiology involves a complex interplay of diastolic dysfunction, systemic inflammation, endothelial dysfunction, and metabolic remodeling within cardiac cells. The study underlines the role of mitochondrial dysfunction as a critical node in this pathology.

Mitochondria, the powerhouse of the cell, play a central role in energy production through oxidative phosphorylation and are particularly important in cardiac myocytes which demand high levels of ATP for contraction and relaxation. In HFpEF, mitochondrial abnormalities—such as reduced biogenesis, impaired electron transport chain activity, and increased reactive oxygen species (ROS) production—contribute to energy deficits and maladaptive remodeling. Tackling these mitochondrial impairments thereby emerges as a potential therapeutic target.

The team focused on nitro-oleic acid, a naturally occurring electrophilic fatty acid nitroalkene formed during oxidative inflammatory processes, noted for its anti-inflammatory and antioxidant properties. Prior studies had hinted at the cardiovascular protective effects of NO2-OA, but its direct impact on mitochondrial function in the context of HFpEF had not been rigorously tested. Using sophisticated in vitro and in vivo models, the researchers meticulously dissected how NO2-OA modulates mitochondrial dynamics and cardiac energetics.

In murine models that recapitulate the hemodynamic and metabolic hallmarks of HFpEF, systemic administration of NO2-OA resulted in marked improvement of diastolic function, demonstrated by echocardiographic parameters and invasive hemodynamic measurements. These functional gains correlated with enhanced mitochondrial respiration rates, increased expression of mitochondrial biogenesis regulators such as PGC-1α, and decreased mitochondrial ROS production. The findings implicate NO2-OA as a modulator that rebalances cardiac energy metabolism.

Delving deeper into the mechanistic underpinnings, the study highlights how NO2-OA impacts mitochondrial electron transport chain complexes, particularly complexes I and IV. NO2-OA treatment led to increased complex activities, favoring improved ATP synthesis efficiency and reduced electron leakage. By minimizing electron leakage, the generation of damaging reactive oxygen species was curtailed, thereby mitigating oxidative stress—a key driver of cardiac dysfunction in HFpEF.

Importantly, the study employed advanced metabolomic profiling to track alterations in cardiac substrate utilization. NO2-OA shifted myocardial metabolism toward enhanced fatty acid oxidation and improved coupling with the tricarboxylic acid (TCA) cycle, reflecting healthier mitochondrial bioenergetics. This metabolic rewiring appears to reverse the maladaptive glycolytic reliance observed in failing hearts, providing a more sustainable ATP supply aligned with myocardial contractile demands.

The authors also examined the influence of NO2-OA on mitochondrial dynamics regulators such as mitofusin 2 and dynamin-related protein 1 (Drp1), proteins controlling mitochondrial fusion and fission, respectively. By reestablishing a balanced mitochondrial network morphology, NO2-OA prevented fragmented and dysfunctional mitochondria in cardiac cells. This restoration of mitochondrial architecture is believed to sustain both respiratory capacity and calcium handling, essential for cardiomyocyte function.

On a molecular signaling level, NO2-OA was found to activate the Nrf2 antioxidant pathway and inhibit NF-κB signaling, thereby attenuating inflammation-driven mitochondrial injury. This dual regulation reinforces a protective milieu conducive to mitochondrial repair and preservation. These anti-inflammatory effects also likely contribute to ameliorating systemic and myocardial inflammation—a known contributor to HFpEF pathogenesis.

Beyond mitochondrial effects, NO2-OA treatment decreased myocardial fibrosis and interstitial collagen deposition, features that are typically exaggerated in HFpEF hearts and contribute to stiffening and impaired relaxation. By intervening early in mitochondrial dysfunction, NO2-OA potentially breaks the vicious cycle of energy deficit, oxidative stress, inflammation, and fibrosis that underpins HFpEF progression.

The translational implications of this study are profound. While NO2-OA or nitro-fatty acid analogs have not yet been clinically tested in HFpEF patients, their endogenous presence and bioactivity suggest therapeutic feasibility. Furthermore, the study proposes that NO2-OA could serve as both a biomarker and a therapeutic agent, offering dual utility in managing HFpEF. This could revolutionize the therapeutic landscape where options currently remain inadequate.

Importantly, the researchers emphasized the need for future investigations to confirm NO2-OA efficacy and safety in larger animal models and human clinical trials. Defining optimal dosing, long-term effects, and patient selection criteria will be pivotal for clinical translation. The study also opens avenues to explore combinatorial approaches integrating NO2-OA with other metabolic modulators or standard-of-care therapies for synergistic benefits.

This seminal work adds compelling evidence to a growing body of literature underscoring the centrality of mitochondrial health in cardiovascular diseases. By targeting mitochondrial metabolism, NO2-OA represents a paradigm shift away from merely symptomatic management toward addressing root causes of metabolic dysfunction in HFpEF. Given the rising prevalence of HFpEF attributable to aging populations and metabolic comorbidities, such advances are urgently needed.

In synopsis, the discovery that nitro-oleic acid can enhance mitochondrial metabolism and rescue diastolic function in heart failure with preserved ejection fraction stands as a beacon of hope for millions affected by this chronic syndrome. The intricate experimental design, rigorous mechanistic elucidation, and promising in vivo results make this study a landmark contribution with potential to spark a new era in cardiovascular therapeutics.

As researchers continue to unravel the nuanced roles of bioactive lipids and mitochondrial signaling in cardiac physiology and pathology, nitro-oleic acid may well emerge as a prototype for next-generation metabolic therapies. Ultimately, the integration of redox biology, mitochondrial dynamics, and immunometabolism in therapeutic development could redefine how we tackle heart failure and related metabolic diseases.

The study has thus not only expanded our understanding of HFpEF pathobiology but also provided a tangible avenue to transform patient outcomes through targeted metabolic interventions. Excitingly, these findings underscore the promise of harnessing nature’s own molecules—like nitro-oleic acid—to unlock the full regenerative and reparative potential of the failing heart.

Subject of Research: The role of nitro-oleic acid in enhancing mitochondrial metabolism and improving cardiac function in heart failure with preserved ejection fraction (HFpEF) in mice.

Article Title: Nitro-oleic acid enhances mitochondrial metabolism and ameliorates heart failure with preserved ejection fraction in mice.

Article References:

Müller, M., Schubert, T., Welke, C. et al. Nitro-oleic acid enhances mitochondrial metabolism and ameliorates heart failure with preserved ejection fraction in mice. Nat Commun 16, 3933 (2025). https://doi.org/10.1038/s41467-025-59192-5

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